Investigation of optimal hernia repair techniques in patients with inflammatory bowel disease.

INTRODUCTION: Multiple laparotomies, immunosuppressive therapy, wound infection, and malnutrition are risk factors for incisional hernia development, which places inflammatory bowel disease (IBD) patients at high risk. With advances in minimally invasive techniques, this study assesses incisional hernia repair techniques and complications in the IBD population. METHODS: A single-center, retrospective review of adults with IBD who underwent incisional hernia repair from 2008 to 2022. Complications relative to operative approach and mesh placement location were assessed using descriptive and univariate statistics. RESULTS: Eighty-eight IBD patients underwent incisional hernia repair. Fifty-two (59.1%) were on immunomodulators and 30 (34.1%) were repaired primarily. Thirty-five (39.7%) hernias recurred, of whom 19 (33%) had mesh placed. Three (30%) occurred in onlay repairs and 16 (33%) occurred in underlay repairs. Subdivision of underlay repairs into intraperitoneal, preperitoneal and retrorectus mesh placement revealed recurrence rates of 35.1%, 50%, and 14.3%, respectively. Patients with open repair were more likely to have intraoperative bowel injury (28.6% vs 9.7%, p = 0.041) and develop postoperative seromas/abscesses (12.5% vs 0%, p = 0.001) and wound complications (17.9% vs 0%, p = 0.012) compared to laparoscopic. Seromas/abscesses developed more frequently in onlay repairs compared to underlay (40% vs 2.13%, p = 0.001). Twelve (13.6%) patients presented with postoperative small bowel obstruction (SBO), 7 (58.3%) of whom had mesh placed, and 6 (85.7%) were underlay. All SBO after underlay repair had intraperitoneally placed mesh. When comparing surgeons, hernias were more likely to recur performed by colorectal surgeons compared to hernia surgeons (63.3% vs 21.3%, p < 0.001). CONCLUSION: In IBD patients, minimally invasive approaches lead to fewer perioperative complications compared to open. Underlay mesh placement demonstrated decreased incidence of seroma/abscess formation compared to onlay. When sub-grouped, underlay placements were similar in terms of complications. Retrorectus placement, however, had fewer recurrences and no readmissions for SBO. This suggests a minimally invasive approach or placement of retrorectus mesh may provide the optimal repair in this patient population.

A Western Massachusetts hospital system's response to the COVID-19 pandemic.

OBJECTIVE: The objective of this paper was to outline a novel model created for the management of the critical care surge due to coronavirus disease 2019 (COVID-19) in a Western Massachusetts hospital. SETTING: This model was created and implemented at a Western Massachusetts Level 1 Trauma and tertiary referral center. CONCLUSIONS: This article outlines a model devised by an interdisciplinary team for rapid expansion of critical care services by increasing allocated space, staffing, and supplies via modifications of existing systems of care to accommodate a predicted large critical care patient surge due to the COVID-19 pandemic. We predict that this model can be utilized and adapted for future critical care surges in times of similar pandemic situations.

HNF1A is a novel oncogene that regulates human pancreatic cancer stem cell properties.

The biological properties of pancreatic cancer stem cells (PCSCs) remain incompletely defined and the central regulators are unknown. By bioinformatic analysis of a human PCSC-enriched gene signature, we identified the transcription factor HNF1A as a putative central regulator of PCSC function. Levels of HNF1A and its target genes were found to be elevated in PCSCs and tumorspheres, and depletion of HNF1A resulted in growth inhibition, apoptosis, impaired tumorsphere formation, decreased PCSC marker expression, and downregulation of POU5F1/OCT4 expression. Conversely, HNF1A overexpression increased PCSC marker expression and tumorsphere formation in pancreatic cancer cells and drove pancreatic ductal adenocarcinoma (PDA) cell growth. Importantly, depletion of HNF1A in xenografts impaired tumor growth and depleted PCSC marker-positive cells in vivo. Finally, we established an HNF1A-dependent gene signature in PDA cells that significantly correlated with reduced survivability in patients. These findings identify HNF1A as a central transcriptional regulator of PCSC properties and novel oncogene in PDA.